We have located links that may give you full text access.
HDAC11 regulates interleukin-13 expression in CD4+ T cells in the heart.
Journal of Molecular and Cellular Cardiology 2018 September
BACKGROUND AND AIMS: Immune deregulation is a causative factor in pathogenesis of myocarditis. Histone deacetylases (HDAC) involve multiple biochemical activities in the cell. This study aims to elucidate the role of HDAC11 in the regulation of interleukin (IL)-13-expression in CD4+ T cells of heart tissue in patients with myocarditis (MCD).
METHODS: After heart transplantation, surgically removed hearts were collected from patients with advanced heart failure and MCD or dilated cardiomyopathy (DCM). CD4+ T cells were isolated from the heart samples and analyzed by immune assay. The association between IL-13 over production by CD4+ T cells in heart tissue and the pathogenesis of MCD was analyzed.
RESULTS: T helper (Th) 2-biased inflammation was observed in hearts tissue of MCD patients with advanced heart failure. CD4+ T cells isolated from MCD heart tissue showed lower levels of HDAC11 expression than that isolated from DCM heart tissue. HDAC11 was negatively correlated with IL-13 expression in the CD4+ T cells. A complex of HDAC11 and E4 binding protein-4 (E4BP4; the transcription factor of IL13) was detected in the CD4+ T cells, which restricted the binding between E4BP4 and the Il13 promoter to repress the Il13 gene transcription. Reconstitution of HDAC11 in MCD CD4+ T cells reduced the expression of IL-13, while inhibition of HDAC11 in DCM CD4+ T cells increased the IL-13 expression.
CONCLUSIONS: HDAC11 is a regulatory molecule in Th2 response and plays a critical role in the restriction of the biased IL-13 expression in CD4+ T cells of the heart.
METHODS: After heart transplantation, surgically removed hearts were collected from patients with advanced heart failure and MCD or dilated cardiomyopathy (DCM). CD4+ T cells were isolated from the heart samples and analyzed by immune assay. The association between IL-13 over production by CD4+ T cells in heart tissue and the pathogenesis of MCD was analyzed.
RESULTS: T helper (Th) 2-biased inflammation was observed in hearts tissue of MCD patients with advanced heart failure. CD4+ T cells isolated from MCD heart tissue showed lower levels of HDAC11 expression than that isolated from DCM heart tissue. HDAC11 was negatively correlated with IL-13 expression in the CD4+ T cells. A complex of HDAC11 and E4 binding protein-4 (E4BP4; the transcription factor of IL13) was detected in the CD4+ T cells, which restricted the binding between E4BP4 and the Il13 promoter to repress the Il13 gene transcription. Reconstitution of HDAC11 in MCD CD4+ T cells reduced the expression of IL-13, while inhibition of HDAC11 in DCM CD4+ T cells increased the IL-13 expression.
CONCLUSIONS: HDAC11 is a regulatory molecule in Th2 response and plays a critical role in the restriction of the biased IL-13 expression in CD4+ T cells of the heart.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
A Guide to the Use of Vasopressors and Inotropes for Patients in Shock.Journal of Intensive Care Medicine 2024 April 14
Diagnosis and Management of Cardiac Sarcoidosis: A Scientific Statement From the American Heart Association.Circulation 2024 April 19
Essential thrombocythaemia: A contemporary approach with new drugs on the horizon.British Journal of Haematology 2024 April 9
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app